The early time course of autophagy in human peripheral blood mononuclear cells following endurance exercise

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The early time course of autophagy in human peripheral blood mononuclear cells following endurance exercise

Author(s)

Lanphere, Kathryn

Advisor(s)

Mermier, Christine

Committee Member(s)

Dokladny, KarolSchneider, SuzanneAnn, GibsonMoseley, Pope

Department

University of New Mexico. Biology Dept.

Degree Level

Doctoral

Abstract

Exercise disrupts homeostasis and leads to the induction of an important catabolic system called autophagy. Autophagy is a beneficial cell survival process that is induced in periods of starvation. The purposes of this study are to (1) determine the time course of autophagy activation following endurance exercise at 70% of VO2max in a warm environment and (2) to determine if exercising at 50% of VO2max induces autophagy in a warm environment. Methods. Eight endurance trained subjects (2 females) participated in this study and completed a moderate intensity exercise (MIE) trial for 1h (50% of VO2max ), and a high intensity exercise (HIE) trial for 1h (70% of VO2max ). Results. Core temperature and heart rate during HIE was higher during 10-60 and 5-60 minutes, respectively, when compared to the same time during MIE and pre-HIE, p < 0.01. IL-6 levels were increased (p < 0.01) 0h post-exercise and 1h post-exercise HIE versus pre-exercise. IL-6 was increased following MIE 0h post-exercise, when compared to pre-exercise, p < 0.01. Decreases (p < 0.05) in plasma insulin were found following HIE at 2h, when compared to pre-exercise. Decreases in plasma insulin were also found at 4h post-exercise following MIE when compared to pre-exercise, p < 0.05. HIE increased (p < 0.05) autophagy marker LC3-II at 0h , 2h, and 4h post-exercise when compared to pre-exercise. MIE increased LC3-II at 1h post-exercise when compared to pre-exercise. LC3b decreased following MIE at 1h (p < 0.01) and was increased at 2h, post-exercise when compared to baseline. HSPA1A was decreased at 1h following HIE, when compared to baseline, p < 0.01. HSP70 and LC3-II were moderately and significantly related during MIE, p < 0.01. Increased Akt phosphorylation occurred 2h post-MIE when compared to pre-exercise levels, p < 0.01. Conclusions. Our data suggest that autophagy can be stimulated by exercise at both 50% VO2max and 70% VO2max. MIE induced phosphorylation of Akt post-exercise and may be activated independent of circulating insulin levels. It is unknown how or if the decreased levels we observed in plasma insulin and increases in IL-6 influence autophagy in PBMCs following exercise.